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Editors Selection IGR 11-1

Bloodflow: Postural change

Comment by Alon Harris on:

15043 Compromised autoregulatory control of ocular hemodynamics in glaucoma patients after postural change, Galambos P; Vafiadis J; Vilchez SE et al., Ophthalmology, 2006; 113: 1832-1836

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While intraocular pressure (IOP) remains the major risk factor for primary open angle glaucoma (POAG), mounting evidence suggests that decreased ocular perfusion pressure is an important risk factor. Faulty retinal and optic nerve head (ONH) blood flow regulation is sug-gested to contribute to retinal ganglion cell death and optic neuropathy observed in POAG. Galambos et al. (1134) have investigated the autoregulatory control of the retrobulbar blood vessels of 20 POAG patients, 20 normal tension glaucoma (NTG) patients and 20 healthy controls in response to postural changes. The ages of all three cohorts were statistically similar which is vital to exclude for the effects of aging on the retrobulbar vasculature.¹

The authors found healthy control subjects have tightly regulated blood flow velocities in the short posterior ciliary arteries supplying the ONH compared to both glaucomatous groups. Ophthalmic (OA) and central retinal artery (CRA) blood flow velocities were found to be dependent upon hydrostatic pressure. This investigation contributes to previous evidence² showing an increased end diastolic velocity and a drop in the resistive index of the OA and CRA of healthy volunteers after reclining.  

The authors did not measure IOP during the two postural settings. This could be an important limitation of their study and may hinder the interpretation of the changes seen in the retrobulbar vessels. Ocular perfusion pressure is calculated as (2/3 MAP-IOP) and has been shown to be an independent risk factor for glaucoma. It is somewhat surprising that systemic blood pressure did not change in the healthy or NTG groups after assuming the supine position, and calculated ocular perfusion pressures would provide critical information on the differing autoregulatory patterns seen among these three cohorts. The authors correctly acknowledge color Doppler imaging assesses blood flow velocities and not actual blood flow and that the vascular alterations might be a secondary effect of optic disc damage rather than the primary causative factor. Despite these limitations, the authors provide further evidence that autoregulatory vascular deficits occur in POAG, specifically in the short posterior ciliary arteries supplying the ONH.

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